In the garden geranium (Pelargonium xhortorum), inbred genotypes resistant to pests (e.g., spider mites and aphids) and inbred genotypes susceptible to pests, have been identified (Gerhold et al., 1984; Walters et al., 1990a) (FIG. 3.1). Pest-resistant and pest-susceptible plants produce anacardic acids (6-alkyl-salicylic acid) in exudates of tall glandular trichomes. However, the composition of anacardic acids differs between resistant and susceptible genotypes (Hesk et al., 1991; Grazzini et al., 1995). The trichome exudate from the resistant genotype has a predominance (.sup..about. 81% of exudate profile) of unsaturated 22:1 .omega..sup.5 and 24:1 .omega..sup.5 anacardic acids. In contrast, trichome exudates from the susceptible genotype lack the .omega..sup.5 products and have saturated 22:0 and 24:0 anacardic acids (FIG. 3.2) (Hesk et al., 1991; Grazzini et al., 1995).
The desaturation status of the anacardic acid exudate affects the physical properties of the exudate and the effectiveness of pest resistance. The anacardic acid exudate of the resistant genotype is fluid and acts as a "sticky trap" that impedes the pest movement and adheres to their exoskeletons (Walters et al., 1990a; Walters et al., 1989). This results in enhanced pest exposure to anacardic acids which have toxic properties and have been shown to inhibit enzymatic steps in pest reproduction (Gerhold et al., 1984; Grazzini et al., 1991). In contrast, the anacardic acid exudate of the susceptible genotype is solid, does not act as an effective "sticky trap", and does not adhere to the exoskeleton; therefore, exposure to the toxic exudate is minimized.
Fatty acids have been shown to be direct precursors of anacardic acids. Saturated and unsaturated .sup.14 C!-labeled fatty acids applied to floral tissue and leaves produce corresponding .sup.14 C!-labeled saturated and unsaturated anacardic acids (Walters et al., 1990b; Hesk et al., 1992). The production of anacardic acids is consistent with the addition of six carbons to the labeled fatty acid (e.g., supplying a 16:0 fatty acid results in the production of a 22:0 anacardic acid) (Walters et al., 1990b; Hesk et al., 1992). Thus the novel 16:1 .DELTA..sup.11 and 18:1 .DELTA..sup.13 fatty acids are direct precursors to the 22:1 .omega..sup.5 and 24:1 .omega..sup.5 anacardic acids (respectively), which are associated with pest resistance (Walters et al., 1990b; Hesk et al., 1992). Consistent with this, the 16:1 .DELTA..sup.11 and 18:1 .DELTA..sup.13 fatty acids and corresponding .omega.5 anacardic acids are specifically localized in the trichomes of the resistant genotype (Hesk et al., 1991; Grazzini et al., 1995; Yerger et al., 1992).
Early analysis of inbred resistant and susceptible genotypes suggested that pest resistance is correlated with a quantitative difference in the levels of .omega.5 anacardic acids (Gerhold et al., 1984; Walters et al., 1990a; Walters et al., 1989; Craig et al., 1986; Walters et al., 1990c). Subsequent refinement of the anacardic acid analysis showed that .omega..sup.5 anacardic acids are either present at high levels in the resistant plants or undetectable in the susceptible plants (Hesk et al., 1991; Grazzini et al., 1995). Analysis of an F.sub.2 population (n=160) resulting from a cross of inbred resistant and inbred susceptible genotypes confirmed a 3:1 segregation ratio (X.sup.2 =0.03, P.gtoreq.0.86) for a single dominant locus controlling the production of .omega..sup.5 anacardic acids (Grazzini, 1993). To confirm the association between .omega..sup.5 anacardic acids and pest resistance, 10 plants containing, and 9 plants lacking, .omega..sup.5 anacardic acids were subjected to mite bioassays. All plants containing .omega..sup.5 anacardic acids were pest-resistant, and all plants deficient for .omega..sup.5 anacardic acids were pest-susceptible (Grazzini, 1993). Accordingly, a need remained both to identify the gene responsible for the pest-resistance as well as the applications of that gene in pest-resistance and other technologies.